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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A persistent hypercalciuria and normal serum levels of calcium were measured in a 5-year-old boy suffering from recurrent macro- and microhaematuria and bilateral nephrolithiasis (stone analysis was positive for calcium-oxalate). No growth retardation or any other relevant clinical parameters concerning hypercalciuria e.g. vitamin D-intoxication or renal tubular acidosis could be observed. A slight secondary hyperparathyroidism and increased calcium excretion during fasting or calcium depleted diet indicates a primary failure of calcium reabsorption as previously described by Bordier (hypercalciuria type 2). Treatment with a combination of hydrochlorothiazide (Esidrix) and sodium chloride depleted diet resulted in a long-lasting normalization of calcium excretion and thus disappearance of symptoms in the child.
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PMID:[Idiopathic hypercalciuria due to primary decrease in the renal tubular reabsorption of calcium. Hypercalciuria type 2 according to Bordier (author's transl)]. 51 92

I. Time has come to distinguish "Bartter syndrome" from "Bartter disease". The latter is an autosomal recessive renal tubulopathy which manifests itself mostly during infancy and childhood. II. Bartter disease is caused neither by a primary renal potassium loss nor by a primary renal hyperprostaglandinism. All evidence is in favor of a defect in the chloride pump located at the thick ascending limb of Henle's loop. III. The most severe expression of Bartter disease is its neonatal form which is characterized by polyhydramnios, premature delivery and a life threatening sodium chloride loss during the early weeks of life. It takes several weeks before sodium wasting turns into renal potassium wasting. IV. Polyhydramnios not associated with echographically detectable fetal malformation is highly suggestive of Bartter disease. Prenatal diagnosis is based on the combination of fetal polyuria and elevated chloride in the amniotic fluid. V. In this setting the administration of indomethacin is useless and even dangerous from the 32nd week of gestation on. Similarly, indomethacin should not be given to the newborn Bartter patient for the first weeks and months of life. Treatment at that stage consist mainly of the administration of large amounts of fluid and sodium chloride. VI. Indomethacin can be used as soon as children with Bartter disease stop growing normally and preferably after the age of 18 months when kidney maturation is established. The daily dose should not exceed 2.5 mg/kg body weight. VII. Hypercalciuria is part of (the neonatal form of) Bartter disease and it is so severe that nephrocalcinosis seems to be the rule. This hypercalciuria is the direct consequence of the chloride reabsorption defect in Henle's loop. Research is needed to find an adequate solution to this problem.
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PMID:[The neonatal form of Bartter's syndrome: current findings in etiology and physiopathology]. 141 86

To assess a possible heritability of a disturbed calcium metabolism in relation to blood pressure regulation, 28 young normotensive offspring of either hypertensive or normotensive parents were studied while administered a defined diet with daily sodium chloride of 6 and 20 g/day for 7 days each. Before the high salt diet was begun, the cytosolic calcium concentration ([Ca2+]i) in platelets was elevated in offspring of hypertensive parents, whereas serum electrolytes, plasma renin activity, plasma catecholamines, and 24-hour urinary excretion of sodium and calcium showed no difference between the two groups. On exposure to a high salt diet, the mean blood pressure increased (from 80 +/- 2 to 85 +/- 2 mm Hg, p less than 0.05) in offspring of hypertensive parents. These changes in mean blood pressure were positively correlated with the basal platelet [Ca2+]i (r = 0.61, p less than 0.01), whereas [Ca2+]i did not demonstrate any significant changes. When the subjects were administered the high salt diet, plasma ionized calcium decreased (from 2.37 to 2.21 meq/l, p less than 0.05) and 1,25-dihydroxyvitamin D3 increased (from 32.7 to 40.8 pg/ml, p less than 0.05) with a transient relative hypercalciuria in offspring of hypertensive parents. This increase of 1,25-dihydroxyvitamin D3 was significantly correlated with the changes in mean blood pressure (r = 0.62, p less than 0.01). Disturbed intraplatelet and systemic calcium metabolism may be of predictive value in the development of hypertension.
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PMID:Disturbed calcium metabolism in offspring of hypertensive parents. 159 47

The effects of salt (sodium chloride) supplementation of rat diets (80 g/kg diet), with or without lactose (150 g/kg), were studied in weanling rats over 14 d. Dietary salt increased water intake and reduced weight gain and food conversion efficiency, but these variables were unaffected by lactose. Salt-supplemented rats exhibited a three- to fivefold increase in urinary calcium excretion and a small increase in urinary magnesium and phosphorus excretion, irrespective of dietary lactose content. In addition, salt supplementation reduced plasma alkaline phosphatase (EC 3.1.3.1) activity. Lactose increased urinary Ca and Mg excretion and plasma Ca and P concentrations. Salt reduced tibia mass but not tibia mass expressed relative to body-weight, but neither variable was affected by lactose. Both tibia Mg content and concentration were reduced by salt but unaffected by lactose, and neither tibia P content nor concentration was affected by salt or lactose. Tibia Ca content was reduced by salt but this was prevented by lactose. Tibia Ca concentration was unaffected by salt or lactose, although there was a reduction (not significant) in tibia Ca concentration in animals fed on the lactose-free diet. These results show that lactose had no independent effect on bone and that reduced accretion of bone mass and mineral content in rats fed on the high-salt diets was due, at least in part, to reduced growth. Failure to offset sodium-induced hypercalciuria by a compensatory increase in net Ca absorption may have contributed to reduced bone Ca accretion. The protective effect of lactose against reduced bone Ca accretion may be due to increased Ca absorption.
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PMID:Effect of dietary lactose on salt-mediated changes in mineral metabolism and bone composition in the rat. 193 8

The case of a 7-year-old boy with the normotensive form of "chloride-shunt" syndrome is described. An unusual feature was the clinical presentation with lithiasis, caused by marked hypercalciuria of renal origin. The present studies were carried out to investigate the nature of the renal tubular defect. Indices for proximal and distal sodium chloride reabsorption were increased during hypotonic saline diuresis. Baseline sodium chloride excretion was low but increased above the range of control values after acute furosemide administration. Baseline potassium excretion was low, was not modified by the infusion of sodium chloride and increased significantly during infusions of sodium sulphate or sodium bicarbonate. Calcium excretion remained unchanged during sodium chloride, sodium sulphate or sodium bicarbonate infusions, but increased after furosemide administration. Nasal insufflation of 1-desamino-8-D-arginine-vasopressin induced both an increase in potassium excretion and a decrease in calcium and magnesium excretion. Plasma atrial natriuretic peptide was increased and was not significantly modified by infusion of hypertonic saline or acute administration of furosemide. These findings indicate that the primary renal abnormality appears to be an enhanced tubular reabsorption of sodium chloride, apparently present in the proximal tubule and the ascending loop of Henle. The associated presence of hypercalciuria also suggests a transport defect in the distal tubule. Decreased potassium excretion probably depends on a voltage-shunting defect in the cortical collecting tubule, which can be reversed by increasing the delivery of non-reabsorbable anions or by enhancing the conductance of the luminal membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:"Chloride-shunt" syndrome: an overlooked cause of renal hypercalciuria. 253 69

Urinary uric acid excretion was assessed in 38 children to determine whether hyperuricuria was a risk factor in children with urolithiasis. Uric acid excretion (measured per deciliter glomerular filtration rate), and fractional excretion of uric acid were similar in 27 children with hypercalciuria and calcium oxalate urinary stones, in six children with idiopathic calcium oxalate urolithiasis, and in five with uric acid urolithiasis, of whom four were white boys and one was an Asian girl. One boy with a urate stone had cystinosis. Serum uric acid concentrations exceeded 6.0 mg/dl (360 mumol/L) in two children with hypercalciuria and in two patients with idiopathic calcium oxalate urolithiasis. None of the children with calcium urolithiasis had excessive urinary excretion of uric acid. In children with hypercalciuria, uric acid excretion did not change significantly when dietary sodium was increased from 1.0 to 5.0 gm/1.73 m2. We conclude that excessive urinary uric acid excretion is seldom an additional risk factor in children with calcium urolithiasis and that dietary sodium chloride does not have a strong influence on urinary excretion of uric acid in children with hypercalciuria.
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PMID:Uric acid excretion in children with urolithiasis. 258 28

Idiopathic hypercalciuria, defined as the urinary excretion of more than 300 mg. calcium per day in men or more than 250 mg. calcium per day in women, or more than 4 mg. calcium per kg. per day, is observed in about 50 per cent of the patients with calcium oxalate/apatite nephrolithiasis and is one of the risk factors for stone formation. These patients do not exhibit hypercalcemia, elevated serum parathyroid hormone concentrations or urinary cyclic adenosine monophosphate excretion nor clinical evidence of sarcoidosis, other granulomas or a malignancy. Hypophosphatemia may be present. Augmented rates of intestinal absorption of dietary calcium account for most of the increments in urinary calcium. Serum 1,25-dihydroxyvitamin D concentrations are in the upper normal range or elevated among many patients and are normal but not suppressed in the others. Activation of 1,25-dihydroxyvitamin D formation may be secondary to hypophosphatemia or other, as yet undefined, factors. Since, 1,25-dihydroxyvitamin D apparently can up-regulate its own receptor, small increments in its synthesis and blood levels could amplify the effect of the hormone to stimulate intestinal calcium absorption. Calcium balances are slightly but significantly negative and urinary hydroxyproline excretion may be increased so that a generalized disorder of calcium homeostasis also involving bone may be present. Additional studies are required to determine the genetic basis for the occurrence of idiopathic hypercalciuria in families, the cause of greater expression of idiopathic hypercalciuria in men and whether environmental factors (high dietary sodium chloride, protein and purified carbohydrate intakes) contribute to the expression of idiopathic hypercalciuria. Although thiazide diuretics, inorganic phosphate, magnesium hydroxide and potassium citrate have provided effective therapy, prospective studies are needed to determine optimum therapy and the optimum duration of treatment.
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PMID:Idiopathic hypercalciuria. 264 29

In rats given desoxycorticosterone (DOC), the recently reported finding that a normal amount of dietary sodium chloride (NaCl) induces hypertension but an equimolar amount of sodium bicarbonate (NaHCO3) does not, might be a consequence of the differing effects of the two sodium salts on the metabolism of calcium. In accord with this hypothesis, we have found that, in uninephrectomized rats given DOC: Dietary NaCl induces persisting hypercalciuria and hypertension whereas an approximately equimolar amount of dietary NaHCO3 induces neither hypercalciuria nor hypertension. The urinary excretion of calcium becomes greater in rats given NaCl than in those given NaHCO3, before their blood pressures become different. Replacing dietary NaCl with a near equimolar amount of dietary NaHCO3 corrects both the hypercalciuria and the hypertension initially induced by NaCl.
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PMID:Dietary chloride as a determinant of disordered calcium metabolism in salt-dependent hypertension. 298 59

Cases of hypomagnesaemia of hereditary renal origin represent at least three different congenital disorders of tubular reabsorption of magnesium (Mg). Isolated familial hypomagnesaemia has been reported in a heterogeneous group of patients and an autosomal dominant pattern of inheritance has often been found to be present. Familial hypokalaemia-hypomagnesaemia, inherited as an autosomal recessive trait, has been reported in 17 patients and we now describe 3 additional cases. Hypomagnesaemia is accompanied by hypokalaemia, metabolic alkalosis, hypocalciuria and moderate sodium chloride wasting. Titration of renal Mg reabsorption indicates the presence of a low threshold but a normal Tm. The inherited defect is probably situated at the level of the distal convoluted tubule and mimics the therapeutic effect of thiazides. This condition is frequently confused with Bartter's syndrome. Familial hypomagnesaemia-hypercalciuria, also inherited as an autosomal recessive trait, has been reported in at least 15 patients and we now add 3 new cases. Hypomagnesaemia is always accompanied by hypercalciuria and nephrocalcinosis. Ocular abnormalities such as myopia and horizontal nystagmus are often present. Hypermagnesiuria is of a greater degree than that observed in the previous entity and reflects a low Tm of Mg reabsorption. The defect must be situated at the level of the ascending limb of the loop of Henle and affects the transport of both calcium and Mg but not of sodium and chloride. This condition has not been clearly separated from hereditary distal renal tubular acidosis in the literature.
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PMID:Hypomagnesaemia of hereditary renal origin. 315 19

Recent studies have shown that, not only in hypertensive animals but even in normotensive rats, dietary salt (sodium chloride) produces a dose-related increase in the left ventricular and renal mass. In the present study the effects of the angiotensin converting enzyme inhibitor (ACEI) enalapril and the thiazide-type diuretic, hydrochlorothiazide, on the development of the salt-induced left ventricular and kidney hypertrophy were examined in normotensive Wistar-Kyoto and Wistar rats. A high intake of sodium chloride (6% of the dry weight of the chow to mimic the level found in many human food items) during eight weeks produced a marked increase in the mass of the left ventricle and the kidneys in both rat strains with little or no effect on blood pressure. The cardiac hypertrophy correlated strongly with the renal hypertrophy. These salt-induced changes in the heart and in the kidneys were completely blocked by hydrochlorothiazide, while enalapril was devoid of any significant effects during the high-salt diet. However, during a low-salt diet enalapril, but not hydrochlorothiazide, effectively lowered the blood pressure and decreased the left ventricular mass of the normotensive rats. There was a 3- to 4-fold increase in the urinary excretion of calcium during the high intake of sodium chloride. Hydrochlorothiazide decreased the urinary excretion of calcium even during the low salt diet, and it completely blocked the salt-induced hypercalciuria. Enalapril had no significant effect on the urinary calcium excretion. During the low-salt diet hydrochlorothiazide increased the calcium and decreased the potassium concentration in the heart while enalapril increased the phosphorus concentration. In conclusion, a high intake of sodium chloride produced hypertrophy both in the heart and in the kidneys, even in the absence of a rise in blood pressure. Salt also remarkably increased the urinary calcium excretion. These harmful effects of salt were blocked by the thiazide diuretic hydrochlorothiazide but not by the ACEI enalapril. However, this study does not allow to make any direct comparison between the effects of enalapril and hydrochlorothiazide.
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PMID:Effects of enalapril and hydrochlorothiazide on the salt-induced cardiac and renal hypertrophy in normotensive rats. 784 79


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